Head injuries can range from minor to severe brain injury. They are a major cause of death and disability worldwide. A head injury occurs when trauma causes injury to the scalp, skull, or brain. Common causes include road traffic accidents and falls. Head injuries are classified based on severity from mild to severe using the Glasgow Coma Scale. Diagnosis involves history, examination, and imaging like CT scan. Management depends on the type and severity of injury but generally involves stabilizing the patient, treating any brain injury, and preventing complications like raised intracranial pressure.

1. HEAD INJURIES
Mizan Kidanu
April 03/2013

2. OUTLINE
Introduction
Epidemiology
Anatomy
Causes
Classification
Diagnosis
Management
Complication

3. INTRODUCTION
A head injury is any trauma that leads to injury
of the scalp, skull, or brain
The injuries can range from a minor bump on
the skull to severe brain injury

4. EPIDEMIOLOGY
Number one killer in trauma
25% of all trauma deaths
50% of all deaths from MVA
200,000 people in the world live with the
disability caused by these injuries
50% in ages b/n 15 and 35

5. ANATOMY

Anatomy of the ’’SCALP’’
Skin
firmly bound to the 3rd layer by
perpendicular fibers
Connective tissue
contain blood vessels of the scalp
Aponeurosis
 fibrous sheet, found over much of
the vertex
attaches occipitalis to frontalis m

6. Loose connective tissue
accounts for the mobility of the scalp
blood tracks freely in this layer bilateral orbital
edema following sever head injury or cranial operation
Periosteum
adheres to the suture lines of the skull
collection of blood beneath this layer  outlines the
affected bone  cephalohematoma (children)

7. Anatomy of the meninges
Dura
endosteum and true meningeal layer
forms falx, tentorium, diaphragm
Arachinoid
vascular membrane
arachinoid granulations
Pia
highly vascular
dips into sulci and fissures
carries cortical vessels

8. CAUSES OF HEAD INJURY
Road traffic accident
65% of deaths following severe
head injury
Falls
Injuries at work place, during
sport, or at home
Assaults

9. CLASSIFICATIONS OF HEAD INJURY
1.
Blunt Vs Penetrating
2.
Primary Vs Secondary
3.
Mild, Moderate, or Severe

10. PRIMARY INJURY TO SCALP
Hematoma - Usually do not require Rx
- If large aspiration when it liquefies
Wounds
Abrasions - Cleaned & exposed
- Dressed - if hemorrhagic or serous
exudates
Lacerations - Cleaned & sutured( LA or GA)
- LA infiltrated into scalp
- Wound closure without tension

11. PRIMARY INJURY TO SKULL
Linear fractures - Do not require Rx
- At temporal area  tear
MMAEDH
Depressed #s - Simple Vs Open
Surgery indicated in:
ocompression (large plate of bone)
ocosmetic area
o compound/open wound:
 wound debridement
 elevate the depression
 suture dural laceration

12.  Fractures of the skull base
Diagnosis
oHistory - nasal bleeding,…
oPhysical examination
Raccoon eyes
Battle sign
Rhinorrhea,......
Management:
conservative, advise on danger Sn
closure of dura - persistent CSF leak

13. PRIMARY BRAIN INJURY
The damage caused to the brain at the moment of
impact
Concussion
 temporary neuronal dysfunction after blunt head trauma
 head CT is normal, & deficits resolve over minutes to hours
Contusion/laceration
 bruise of the brain
 breakdown of small vessels and extravasation
of blood into the brain
Diffuse axonal injury
 damage to axons throughout the brain
 most frequent finding in patients who die from severe head injury

14. Mechanisms
Coup & counter-coup injuries
 Common sites:-
undersurface of frontal lobe
tip of temporal lobe

15. SECONDARY BRAIN INJURY
Extracranial
 hypoxia
 hypotension
Intracranial




hematoma
brain edema
raised ICP
infection

16. DIAGNOSIS
History
 Age
 Loss of consciousness
 Cause, circumstance and mechanism of
injury
 Presence of headache & vomiting
 Seizures
 Anticoagulant use,….

17. ASSESSMENT OF NEUROLOGICAL FUNCTION
AND OF CONCIOUS LEVEL
Glasgow Coma Score
Best Eye Response (4)
No eye opening……………………………1
Eye opening to pain..…………………….2
Eye opening to verbal command.……...3
Eyes open spontaneously…...………….4
Best Verbal Response (5)
No verbal response ………………………1
Incomprehensible sounds. ……………..2
Inappropriate words. …………………….3
Confused …………………………………..4
Orientated …………………………………5
Best Motor Response (6)
No motor response.…………………..…..1
Extension to pain.…………………….…..2
Flexion to pain.……………………….…...3
Withdrawal from pain..……………….…..4

18. Classification of head injury
Mild: GCS = 13-15
Moderate: GCS = 9-12
Severe: GCS = 3-8

19. Exclude other causes of depressed
conscious level (causes of coma)
No focal signs
drugs (alcohol, opiate)
circulatory collapse
hypothermia / hyperthermia
concussion
meningitis, encephalitis
subarachinoid hemorrhage
Focal signs present
cerebral abscess ,infarction, tumor
intracranial hemorrhage

20. Investigations
Skull radiograph
CXR and X-ray of cervical spines
CT-Scan - first line investigation

21. Indication for CT-scan
 GCS<13 at any stage
 GCS =13 or 14 at 2 hours following injury
 Suspected open or depressed #
 Any sign of basal skull #
 Post-traumatic seizures
 Focal neurologic deficit
 Post-traumatic amnesia of >30 minutes
 Persistent vomiting
 Coagulopathy
 Significant mechanism of injury

22. GENERAL MANAGEMENT OF HEAD INJURY
ABC rule
stabilization of airway, breathing and circulation
IV access - maintain normovolemia
- hypotonic/glucose containing fluids
should not be used
endotracheal intubation (e.g: GCS ≤ 8, hypoxia,…)
Head end elevation - 300
Treat co-existing injuries
chest drain - tension pneumothorax
cervical collar - # of cervical spine,….

23. Anticonvulsants
may decrease early posttrauma seizures but
no benefit in long term epilepsy prevention
Phenytoin
 Loading dose = 18 - 20 mg/kg
 Maintenance dose = 100 mg q 8 hrly

24. Regular observation at half hourly interval:
GCS
BP, HR, RR, and Temperature
oxygen saturation
pupil size & reactivity
limb movement

25. EPIDURAL HEMATOMA
Usually from torn middle meningeal artery
and/or vein
Other causes:
torn dural sinuses(e.g: saggital sinus)
oozing from diploe bone & stripped dura
Uncommon but serious,1- 4% of TBI
Highest among adolescents and young adults
Skull fractures in 75-95%

26. Clinical presentation
lucid interval (in 1/3 of cases) associated with
headache vomiting, drowsiness, confusion,
aphasia, seizures and hemiparesis
epidural hematoma due to venous bleeding
neurologic decline is slower
posterior fossa EDH - elevated ICP

27. Diagnostic evaluation
 CT scan - lens shaped collection
- hematoma volume
estimation
Management
 craniotomy / ?burr hole
Prognosis-mortality -10%

28. SUBDURAL HEMATOMA
Pathophysiology
result from the tearing of bridging veins crossing
the subdural space or hemorrhage from severe
cerebral contusions
Spread more diffusely over the hemisphere
than extradural and are often associated with
diffuse swelling of the underlying hemisphere
Clinical manifestations - depends on type

29. ACUTE SUBDURAL HEMATOMA
1-2 days after onset
coma in (56%)
lucid interval (12-38%)
posterior fossa SDH - signs of increased ICP
Result from:
torn bridging veins
cortical lacerations
torn dural sinuses

30. CT SCAN FEATURES
clot is bright or mixed-density
crescent-shaped (lunate)
may have a less distinct border
does not cross the midline due to
the presence of falx
Signs of mass effect:
ventricular compression, midline
shift and reduction in the size of
the basal cisterns

31. SUBACUTE SUBDURAL HEMATOMA
After approximately 1-2 weeks the subdural
collection become isodense to grey matter
detection may be challenging & recognized when:
 effacement of cortical sulci
 deviation of lateral ventricle
 midline shift
Contrast enhancement will often define cortical-
subdural interface

32. CHRONIC SUBDURAL HEMATOMA
after 2 weeks usually post trivial injury
due to injury of small bridging veins
headache, cognitive impairment, apathy,
seizures and focal deficits
symptoms are transient and fluctuating
proximal, painless and intermittent
paraparesis

33. CT features
 After 2 weeks, hypodense
crescentic collections
 Acute-on-chronic SDHs can
further complicate the images,
with hyperdense fresh
haemorrhage intermixed, or
layering posteriorly, within the
chronic collection
 Do not cross the midline

34. Management
Acute SDH - Surgery for symptomatic & unstable pt
 Surgery
burr hole
craniotomy
 Nonoperative Mx
clinically stable
clot thickness <10mm
no clinical or CT signs of herniation
repeat CT scans 6-8 hrs after initial scan

35. Chronic SDH
Surgery - burr hole
signs of increased ICP
clot thickness >10mm
cognitive impairment
motor impairment

36. RAISED INTRACRANIAL PRESSURE
The three normal contents
of the cranial vault are brain
tissue (80%), blood (10%),
and CSF (10%)
Normal state - ICP normal
4-14 mmHg - normal
>20mmHg – abnormal

37. The Monro-Kellie doctrine states that ’’the cranial
vault is a rigid structure, and therefore, the total
volume of the contents determines ICP ’’
Cerebral Perfusion Pressure (CPP) can be
determined by the following formula:
CPP = MAP – ICP

38. Symptoms & Signs of increased ICP

Diminishing level of consciousness

Headache, vomiting, seizures

Cushing’s Triad:
 bradycardia
 hypertension
 abnormal respiration

Pupillary changes

Papilledema

39. Effects of raised ICP:
brain herniation
1. subfalcine herniation
2. uncal herniation
3. central transtentorial
herniation
4. tonsillar herniation
reduced cerebral perfusion

40. Management of raised ICP
includes airway protection and adequate
ventilation (intubation may be required)
a bolus of Mannitol 0.25-1g/kg causes:
free water diuresis
increased serum osmolality and extraction
of water from the brain
require rapid neurosurgical evaluation
ventriculostomy or craniotomy may be
needed for definitive decompression

41. COMPLICATIONS HEAD INJURY
Meningitis & brain abscess
CSF rhinorrhea
and otorrhea
Epilepsy - about 80% arise in 2yrs
Hydrocephalus- usually due to atrophied white
matter
Amnesia (PTA)
Postconcussional Sx
Posttraumatic encephalopathy
Cranial nerve injury - in up to 30% pts

42. REFERENCES
Mark S. Greenberg: Hand Book of Neurosurgery; 6th
ed
Bailey & Love’s: Short Practice of Surgery; 24th ed,
2004
Peter J Morris: Oxford Text Book of Surgery; 2nd ed,
2002
Schwartz's: Principles of Surgery; 9th ed, 2010